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Interferon-stimulated gene 56 positively regulates Toll-like receptor 3-mediated CXCL10 expression in human renal proximal tubular epithelial cells.
Tachizaki, Mayuki; Sakamoto, Sho; Kobori, Yuri; Asano, Yoshiya; Kawaguchi, Shogo; Seya, Kazuhiko; Tanaka, Hiroshi; Morita, Eiji; Imaizumi, Tadaatsu.
Afiliación
  • Tachizaki M; Department of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Japan.
  • Sakamoto S; Department of Biochemistry and Molecular Biology, Hirosaki University Faculty of Agriculture and Life Science, Japan.
  • Kobori Y; Department of Respiratory Medicine, Hirosaki University Graduate School of Medicine, Japan.
  • Asano Y; Department of Neuroanatomy, Cell Biology and Histology, Hirosaki University Graduate School of Medicine, Japan.
  • Kawaguchi S; Department of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Japan.
  • Seya K; Department of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Japan.
  • Tanaka H; Department of School Health Science, Hirosaki University Faculty of Education, Japan.
  • Morita E; Department of Biochemistry and Molecular Biology, Hirosaki University Faculty of Agriculture and Life Science, Japan.
  • Imaizumi T; Department of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Japan.
FEBS Open Bio ; 14(8): 1303-1319, 2024 Aug.
Article en En | MEDLINE | ID: mdl-38923445
ABSTRACT
Viral infections in tubular epithelial cells lead to the production of inflammatory cytokines by innate immunity, causing tubulointerstitial nephritis. TLR3 recognizes viral infections and acts via the activation of interferon (IFN)/IFN-stimulated genes (ISGs). This study investigates the role of ISG56, a representative ISG, in TLR3 signaling in cultured human renal proximal tubular epithelial cells (hRPTECs). To this end, hRPTECs were stimulated by a synthetic TLR3 ligand, polyinosinic-polycytidylic acid (poly IC), recombinant human interferon-ß [r(h)IFN-ß] or Japanese encephalitis virus (JEV) infection and assayed for inflammatory cytokine mRNA expression by RT-qPCR, and protein expression via western blotting or ELISA. ISG56 was expressed by poly IC or r(h)IFN-ß and IFN-ß knockdown reduced poly IC-induced expression of ISG56 and CXCL10. Moreover, ISG56 knockdown reduced poly IC- or r(h)IFN-ß-induced expression of CXCL10 at the same time as increasing JEV growth and reducing CXCL10 expression induced by JEV infection. Overall, TLR3 signaling induced IFN-ß-dependent expression of ISG56 and CXCL10. We show that ISG56 possibly plays a critical role in antiviral immunity of hRPTECs by positive regulation of IFN-ß-mediated CXCL10 expression downstream of TLR3.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Interferón beta / Células Epiteliales / Receptor Toll-Like 3 / Quimiocina CXCL10 / Túbulos Renales Proximales Límite: Humans Idioma: En Revista: FEBS Open Bio Año: 2024 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Interferón beta / Células Epiteliales / Receptor Toll-Like 3 / Quimiocina CXCL10 / Túbulos Renales Proximales Límite: Humans Idioma: En Revista: FEBS Open Bio Año: 2024 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido